A comparative assessment of mitochondrial function in epimastigotes and bloodstream trypomastigotes of <Emphasis Type="Italic">Trypanosoma cruzi</Emphasis> |
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| Authors: | Renata L S Gonçalves Rubem F S Menna Barreto Carla R Polycarpo Fernanda R Gadelha Solange L Castro Marcus F Oliveira |
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| Institution: | 1.Laboratório de Bioquímica de Resposta ao Estresse, Programa de Biologia Molecular e Biotecnologia,Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro,Rio de Janeiro,Brazil;2.Laboratório de Inflama??o e Metabolismo,Instituto Nacional de Ciência e Tecnologia de Biologia Estrutural e Bioimagem (INBEB), Universidade Federal do Rio de Janeiro,Rio de Janeiro,Brazil;3.Laboratório de Biologia Celular,Instituto Oswaldo Cruz, FIOCRUZ,Rio de Janeiro,Brazil;4.Laboratório de Biologia Molecular, Programa de Biologia Molecular e Biotecnologia,Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro,Rio de Janeiro,Brazil;5.Departamento de Bioquímica,Instituto de Biologia, Universidade Estadual de Campinas,Campinas,Brazil |
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| Abstract: | Trypanosoma cruzi is a hemoflagellate protozoan that causes Chagas’ disease. The life cycle of T. cruzi is complex and involves different evolutive forms that have to encounter different environmental conditions provided by the
host. Herein, we performed a functional assessment of mitochondrial metabolism in the following two distinct evolutive forms
of T. cruzi: the insect stage epimastigote and the freshly isolated bloodstream trypomastigote. We observed that in comparison to epimastigotes,
bloodstream trypomastigotes facilitate the entry of electrons into the electron transport chain by increasing complex II-III
activity. Interestingly, cytochrome c oxidase (CCO) activity and the expression of CCO subunit IV were reduced in bloodstream forms, creating an “electron bottleneck”
that favored an increase in electron leakage and H2O2 formation. We propose that the oxidative preconditioning provided by this mechanism confers protection to bloodstream trypomastigotes
against the host immune system. In this scenario, mitochondrial remodeling during the T. cruzi life cycle may represent a key metabolic adaptation for parasite survival in different hosts. |
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